Norovirus Gastroenteritis, Carbohydrate Receptors, and Animal Models

Division of Infectious Diseases, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America.
PLoS Pathogens (Impact Factor: 7.56). 08/2010; 6(8):e1000983. DOI: 10.1371/journal.ppat.1000983
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    • ", 2013 ) . On the other hand , an individual ' s susceptibility to NoVs is correlated with his HBGA profile in vivo ( Tan and Jiang , 2010 ; Ruvoën - Clouet et al . , 2013 ) . "
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    ABSTRACT: This study aims to investigate if histo-blood group antigen (HBGA) expressing bacteria have any protective role on human norovirus (NoV) from acute heat stress. Eleven bacterial strains were included, belonging to Escherichia coli, Enterobacter cloacae, Enterobacter aerogenes, Clostridium difficile, Bifidobacterium adolescentis, and B. longum. HBGA expression of the bacteria as well as binding of human NoV virus-like particles (VLPs, GI.1, and GII.4 strains) to the bacteria were detected by flow cytometry. NoV VLPs pre-incubated with HBGA expressing or non-HBGA expressing bacteria were heated and detected by both direct ELISA and porcine gastric mucin-binding assay. The NoV-binding abilities of the bacteria correlated well with their HBGA expression profiles. Two HBGA expressing E. coli (LMG8223 and LFMFP861, both GI.1 and GII.4 binders) and one non-HBGA expressing E. coli (ATCC8739, neither GI.1 nor GII.4 binder) were selected for the heat treatment test with NoV VLPs. Compared with the same cell numbers of non-HBGA expressing E. coli, the presence of HBGA-expressing E. coli could always maintain higher antigen integrity, as well as mucin-binding ability of NoV VLPs of both GI.1 and GII.4 after heat-treatment at 90°C for 2 min. These results indicate that HBGA-expressing bacteria may protect NoVs during the food processing treatments, thereby facilitating their transmission.
    Frontiers in Microbiology 07/2015; 6:659. DOI:10.3389/fmicb.2015.00659 · 3.99 Impact Factor
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    • "ORF2 is approximately 1.8 kb and encodes the 57 kDa major capsid protein, VP1, while ORF3 is approximately 0.6 kb and encodes a 33 kDa minor structural protein, VP2 (McFadden et al., 2011). VP1 is suggested to be involved in the recognition of the host cell receptor (Tan & Jiang, 2010) while VP2 is thought to be involved in the stability of the capsid but also seems to be vital for viral assembly (Glass et al., 2009). Recent studies have shown that murine norovirus has an additional ORF, ORF4, which overlaps ORF2 in an alternate reading frame (Thackray et al., 2007). "
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    ABSTRACT: Diarrhea is considered to be the second leading cause of death due to infections among children <5 years of age worldwide that may be caused by bacteria, parasites, viruses and non-infectious agents. The major causative agents of diarrhea in developing countries may vary from those in developed countries. Noroviruses are considered to be the most common cause of acute diarrhea in both children and adults in industrialized countries. On the other hand, there is lack of comprehensive epidemiological evidence from developing countries that norovirus is a major cause of diarrhea. In these regions, asymptomatic norovirus infections are very common, and similar detection rates have been observed in patients with diarrhea and asymptomatic persons. This review summarizes current knowledge of norovirus infection in developing countries and seeks to position infections with noroviruses among other enteropathogens as disease burden in these regions.
    Journal of General Virology 05/2015; 96(8). DOI:10.1099/vir.0.000194 · 3.18 Impact Factor
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    • ". ORF2 and ORF3 encode a viral capsid protein (VP1) and a minor capsid protein (VP2), respectively, the latter of which serves to stabilize VP1 [Jiang et al., 1993]. The functional domain of NoV VP1 is composed of a shell (S) and two protruding (P) domains, P1 and P2 [Tan et al., 2003; Lindesmith et al., 2008; Tan and Jiang, 2010]. The S and P1 domains are relatively conserved within a given genotype of NoV. "
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    ABSTRACT: The incidence of noroviral gastroenteritis has increased dramatically in recent years, and norovirus (NoV) genogroup II.4 (GII.4) is associated with outbreaks worldwide. The NoV genotypes and their clinical relevance in children hospitalized with acute gastroenteritis between 2006 and 2011 in northern Taiwan were evaluated in this study. NoV sequences were amplified from 47 clinical specimens and phylogenetic analysis was performed. Based on noroviral capsid protein (VP1) and RNA dependent RNA polymerase (RdRp) phylogeny, circulating NoV could be divided into GII.2, GII.3, GII.12, and GII.4 and GII.16, GII.12, GII.g, and GII.4; respectively. The GII.4 subtype was predominant and could be divided further into the 2004 (Hunter), 2006b, and 2010 (New Orleans) subtypes. Regarding clinical manifestations, convulsive disorder occurred only in cases caused by NoV GII.4 2006b. Patients affected by NoV GII.4 2006b presented with a higher frequency of diarrhea (P = 0.0204), longer duration of diarrhea (P = 0.0215), more frequent hypoglycemia (P = 0.038), and electrolyte imbalance (P = 0.0487) than acute gastroenteritis caused by NoV GII.4 2010. Structural analysis showed that the amino acid changes in viral VP1 between GII.4 2006b and 2010 subtype were located mainly in the protruding domain 2 (P2 domain). In conclusion, the NoV GII.4 variants 2006b and 2010 were the main causes of acute gastroenteritis in hospitalized children in northern Taiwan during 2006-2011. The clinical presentations and structural changes in VP1 of the two NoV GII.4 variants should be evaluated in the future. J. Med. Virol. © 2013 Wiley Periodicals, Inc.
    Journal of Medical Virology 02/2014; 86(2). DOI:10.1002/jmv.23728 · 2.35 Impact Factor
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